a. Field of the Invention
The instant invention relates generally to the reduction and prevention of arrhythmias, such as atrial fibrillation. More specifically, the instant invention relates to apparatus and methods for reducing and preventing arrhythmias using photobiomodulation therapy, either alone or in conjunction with other therapies.
b. Background Art
In photobiomodulation therapy, laser light is applied to tissue in order to address an abnormal tissue response. In general, photobiomodulation can be described as the use of light to induce a biological response in living cells and tissue as a direct result of the absorbance of light by the living cells and tissue.
One widespread and widely accepted use of photobiomodulation therapy is for the reduction of pain. For example, photobiomodulation has been shown to reduce pain associated with acute inflammation, for example resulting from acute ankle sprains, acute Achilles tendonitis, and oral surgery. In these circumstances, photobiomodulation therapy is presumed to exert anti-inflammatory effects, for example by reducing the levels of prostaglandin E2, tumor necrosis factor-α, and interleukin-1.
It is widely accepted that some of the effects of photobiomodulation are exerted through interaction between the laser light and an enzyme, cytochrome c oxidase, present in mitochondria. This enzyme functions as a photoacceptor for light of certain wavelengths. After absorption of light, energy transfer occurs. Cytochrome c oxidase is the last enzyme in the cellular respiratory chain and is crucial for the formation of ATP which, in turn, provides energy for biochemical processes such as muscle contraction and metabolic reactions. For example, larger numbers of non-damaged mitochondria as well as higher levels of ATP have been observed in the ischemic zone after myocardial infarction in animals treated with photobiomodulation therapy as compared to untreated animals.
Atrial fibrillation is one of the most common cardiac arrhythmias, affecting millions of people worldwide. The economic stress of atrial fibrillation on the health care system is enormous, and, as the western population grows older, the number of atrial fibrillation patients is predicted to rise.
It is known that atrial fibrillation results from disorganized electrical activity in the heart muscle (the myocardium). The underlying causes of atrial fibrillation, however, are not completely understood, though it is understood that hypertensive patients are at a higher risk of developing atrial fibrillation.
It is also known that angiotensin II causes inflammation and vice versa. Further, the induction of atrial fibrosis is angiotensin II dependent, and atrial fibrosis is thought to be one of the mechanisms causing atrial fibrillation. Indeed, human atrial tissue expression of angiotensin II receptors have been linked with increased cell death and leukocyte infiltration. This may demonstrate a potential link between the renin-angiotensin-aldosterone system (“RAAS”), inflammation, and atrial fibrillation. As known, RAAS inhibition has desirable effects, both in primary and secondary prevention of atrial fibrillation.